Figure 2.

Experiments performed in the early 1990s using the MYC transactivation domain (TAD) fused to the DNA binding domain of GAL4 in promoter/reporter assays suggested that the activity of the MYC TAD was enhanced by serum stimulation or by ERK2, and was regulated during the cell cycle in a Ser-62 dependent manner [54,89]. The mammalian cell cycle. The cell cycle phases, gap 1 (G1), DNA synthesis (S), gap 2 (G2) and mitosis (M) and the different cyclin/cyclin-dependent kinase (CDK) complexes and their periods of activity during the cell are illustrated. The retinoblastoma protein (pRB), which blocks entry into S phase through transcriptional repression of E2F family transcription factors, is inactivated by D-type/E-type-cyclin/CDK2/4/6 phosphorylation thus enabling G1-S phase transition. The activities of the CDK2 and CDK1 complexes are inhibited by the CDK inhibitor p27^KIP1 (p27). The points of intervention by MYC in the cell cycle are depicted. Proteins depicted in black represent factors with growth-promoting/oncogenic function (with the exception of MYC, which is colored blue), while those in orange represent growth/tumor-suppressive function in this context.